1. Intracellular recordings were made from stage 2 expiratory bulbospinal neurons (E2Ns) in the caudal part of the ventral respiratory group in pentobarbitone-anesthetized cats, to characterize changes in neuronal input resistance (Rn) and synaptic inhibition occurring at the time of the expiratory-inspiratory phase transition of the respiratory cycle. 2. Rn was maximal between 30-90% of stage 2 expiration, but decreased significantly during the last 10% of stage 2 expiration. Mean normalized Rn for 60-90% of stage 2 expiration was 0.9 +/- 0.02, while mean Rn during the last 10% of stage 2 expiration was 0.68 +/- 0.09 (n = 8). This decrease in Rn began 200-300 ms before rapid hyperpolarization of E2N membrane potential and onset of phrenic nerve activity. 3. Under conditions of strong central respiratory drive, constant injection of positive current into E2Ns sometimes revealed a transient membrane hyperpolarization that straddled the expiratory-inspiratory phase transition. During this transient event, Rn was markedly reduced. 4. Intracellular injection of Cl- or NO3- ions into E2Ns produced reversal of chloride-dependent inhibitory synaptic potentials (IPSPs). Comparison of averages of membrane potential pattern over the whole respiratory cycle during control conditions and IPSP reversal revealed several periods of synaptic inhibition: 1) weak but progressively increasing synaptic inhibition during the second half of stage 2 expiration, 2) strong transient synaptic inhibition beginning 200-300 ms before the onset of phrenic nerve activity and ending shortly after the onset of phrenic nerve activity, and 3) strong but progressively decreasing synaptic inhibition throughout inspiration.(ABSTRACT TRUNCATED AT 250 WORDS)